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Brain Under Stress and Alzheimer’s Disease

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Abstract

Modern society is characterized by the ubiquity of stressors that affect every individual to different extents. Furthermore, experimental, clinical, and epidemiological data have shown that chronic activation of the stress response may participate in the development of various somatic as well as neuropsychiatric diseases. Surprisingly, the role that stress plays in the etiopathogenesis of Alzheimer’s disease (AD) has not yet been studied in detail and is therefore not well understood. However, accumulated data have shown that neuroendocrine and behavioral changes accompanying the stress response affect neuronal homeostasis and compromise several key neuronal processes. Mediators of the neuroendocrine stress response, if elevated repeatedly or chronically, exert direct detrimental effects on the brain by impairing neuronal metabolism, plasticity, and survival. Stress-induced hormonal and behavioral reactions may also participate in the development of hypertension, atherosclerosis, insulin resistance, and other peripheral disturbances that may indirectly induce neuropathological processes participating in the development and progression of AD. Importantly, stress-induced detrimental effects as etiological factors of AD are attractive because they can be reduced by several approaches including behavioral and pharmacological interventions. These interventions may therefore represent an important strategy for prevention or attenuation of the progression of AD.

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Acknowledgements

This work was supported by the Slovak Research and Development Agency under the contract No. APVV-0088-10 and European Regional Development Fund Research and Development Grant (ITMS 26240120015). We wish to thank Dr. Ken Goldstein of ScienceDocs (www.sciencedocs.com) for the editing of this paper.

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BM drafted the manuscript, LH and AP helped to revise and finalize the manuscript.

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Correspondence to Boris Mravec.

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Mravec, B., Horvathova, L. & Padova, A. Brain Under Stress and Alzheimer’s Disease. Cell Mol Neurobiol 38, 73–84 (2018). https://doi.org/10.1007/s10571-017-0521-1

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